Platelet PlA2 polymorphism enhances risk of neurocognitive decline after cardiopulmonary bypass

Background. Neurocognitive decline, often produced by atherosclerotic plaque embolization, remains a frequent complication of cardiopulmonary bypass. Plaque fragments may initiate local thrombosis, which, in turn, aggravates the embolic insult. Prothrombotic genetic factors may exacerbate this process. We investigated whether the Pl(A2) polymorphism of platelet GPIIIa, a prothrombotic risk factor in other cardiovascular settings, is associated with early neurocognitive decline after cardiopulmonary bypass. Methods. Neurocognitive changes were evaluated by the Mini-Mental State Examination administered preoperatively and on postoperative day 4 and the PIA genotype determined in 70 patients undergoing cardiopulmonary bypass. Results. Forty-nine patients were Pl(A1/A1), and 21 were Pl(A1/A2) or Pl(A1/A2). Fifty-two patients (74%) demonstrated post-cardiopulmonary bypass neurocognitive decline, of which 34 were Pl(A1/A1) and 18 were Pl(A1/A2) or Pl(A2/A2) Multivariate analysis revealed that the Pl(A2) genotype and baseline Mini-Mental State Examination were significantly associated with greater neurocognitive decline (decreased Mini-Mental State Examination scores, p = 0.036 and 0.024, respectively). Conclusions. This study demonstrates a link between the Pl(A2) allele of platelet GPIIIa and more severe neurocognitive decline after cardiopulmonary bypass. Although the mechanism is unknown, it could represent exacerbation of platelet-dependent thrombotic processes associated with plaque embolism. (C) 2001 by The Society of Thoracic Surgeons.